Medical Neuroscience explores the functional organization and neurophysiology of the human central nervous system, while providing a neurobiological framework for understanding human behavior. In this course, you will discover the organization of the neural systems in the brain and spinal cord that mediate sensation, motivate bodily action, and integrate sensorimotor signals with memory, emotion and related faculties of cognition. The overall goal of this course is to provide the foundation for understanding the impairments of sensation, action and cognition that accompany injury, disease or dysfunction in the central nervous system. The course will build upon knowledge acquired through prior studies of cell and molecular biology, general physiology and human anatomy, as we focus primarily on the central nervous system.
This online course is designed to include all of the core concepts in neurophysiology and clinical neuroanatomy that would be presented in most first-year neuroscience courses in schools of medicine. However, there are some topics (e.g., biological psychiatry) and several learning experiences (e.g., hands-on brain dissection) that we provide in the corresponding course offered in the Duke University School of Medicine on campus that we are not attempting to reproduce in Medical Neuroscience online. Nevertheless, our aim is to faithfully present in scope and rigor a medical school caliber course experience.
This course comprises six units of content organized into 12 weeks, with an additional week for a comprehensive final exam:
- Unit 1 Neuroanatomy (weeks 1-2). This unit covers the surface anatomy of the human brain, its internal structure, and the overall organization of sensory and motor systems in the brainstem and spinal cord.
- Unit 2 Neural signaling (weeks 3-4). This unit addresses the fundamental mechanisms of neuronal excitability, signal generation and propagation, synaptic transmission, post synaptic mechanisms of signal integration, and neural plasticity.
- Unit 3 Sensory systems (weeks 5-7). Here, you will learn the overall organization and function of the sensory systems that contribute to our sense of self relative to the world around us: somatic sensory systems, proprioception, vision, audition, and balance senses.
- Unit 4 Motor systems (weeks 8-9). In this unit, we will examine the organization and function of the brain and spinal mechanisms that govern bodily movement.
- Unit 5 Brain Development (week 10). Next, we turn our attention to the neurobiological mechanisms for building the nervous system in embryonic development and in early postnatal life; we will also consider how the brain changes across the lifespan.
- Unit 6 Cognition (weeks 11-12). The course concludes with a survey of the association systems of the cerebral hemispheres, with an emphasis on cortical networks that integrate perception, memory and emotion in organizing behavior and planning for the future; we will also consider brain systems for maintaining homeostasis and regulating brain state.

Рецензии

RR

While I greatly respect Dr. White's obvious immense knowledge of the neural anatomy, I feel taking this course did very little beyond showing me that perhaps medicine and anatomy wasn't for me.

SJ

Jun 27, 2017

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I've always wanted to attend a course like this which offers such a detailed description of the fundamentals of neuroscience. Glad I found it and sure as hell recommended it to all my friends.

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Movement and Motor Control: Lower and Upper Motor Neurons

We come now to another pivot in Medical Neuroscience where our focus shifts from sensation to action. Or to borrow a phrase made famous by C.S. Sherrington more than a century ago (the title of his classic text), we will now consider the “integrative action of the nervous system”. We will do so in this module by learning the basic mechanisms by which neural circuits in the brain and spinal cord motivate bodily movement.

Преподаватели

Leonard E. White, Ph.D.

Текст видео

Welcome back to this tutorial on lower motor neuronal control of movement. In this part, I'd like to talk about segmental reflexes of the spinal cord. So, the learning objectives that pertain to this part of our tutorial are several. I want you to be able to discuss the critical components of the myotatic reflex and how they interact to monitor and adjust muscle length. I want you to be able to characterize the role of gamma motor neurons in the adjustment of the gain of our muscle spindle system. I want you to be able to discuss the factors that account for muscle tone. I want you to be able to discuss the critical components of the Golgi tendon reflex and how they interact to monitor and adjust the force of muscle contraction. We'll spend a bit of time talking about the difference between the contributions of the muscle spindle. And the Golgi tendon organs to the control of muscle activity, so that will be a, a key point of differentiating learning objective number two from learning objective number four. And then finally I want you to be able to discuss the critical components of another type of reflex called the flexion or the crossed-extension reflex, and how these components interact to withdraw a limb from a harmful stimulus. Okay, so let's begin by talking about a reflex, the simplest of all reflexes that we have through the circuits of our central nervous system. It's called the myotatic reflex, perhaps you better know this as the stretch reflex. The stretch reflex or the myotatic reflex is a system that monitors and maintains the length of a muscle. And the way this system works is through a beautiful organ that we find within our muscles of our muscular skeletal system. And this structure is called the muscle spindle. So, the muscle spindle is a collection of muscle fibers that are found within a capsule. And so, the boundary of these specialized muscle fibers by this capsule allows the anatomists to call these intrafusal muscle fibers. this idea of a fusi, fusiform shape describes the shape of this muscle spindle or rather the capsule that surrounds these muscle fibers. So, there are indeed muscle fibers within the capsule but these are very specialized muscle fibers that are innervated by sensory axons. So, here to the right on the slide, we see our muscle spindle, which is this structure bounded by the capsule and within that muscle spindle, we see some number of specialized muscle fibers. And those would be our intrafusal muscle fibers. And notice that there are a number of axons that are associated with this muscle spindle. There are two types of sensory axons, there's the group 1A, afferent axon and the group two afferent axon. The group 1A tends to supply the central portion of these intrafusal muscle fibers, which is where the nuclei of these muscle fibers tend to aggregate. The group two afferent axon supplies the contractile portions of these intrafusal muscle fibers, which is found away from that more bulbous shaped central region. And rather than wrapping around these muscle fibers in a spiral type shape, which is what happens in group one axons, the group two axons, they make a more limited type of ending that we call the flower spray ending. And the flower spray ending is intended to imply to the microanatomists that the terminals look like petals of a flower that are blossoming on the contractile elements of these intrafusal muscle fibers. There's also a motor supply to the contractile portion of the intrafusal muscle fibers. And this is from a small motor neuron that we find in the ventral horn of the spinal cord, this is called a gamma motor neuron. And we'll come back and talk about the critical role of the gamma motor neurons, in adjusting the sensitivity of this muscle spindle to changes in the length of the muscle. Let me back up just a moment, and say a little bit more about these intrafusal muscle fibers. They basically come in two varieties, so there are a group of morphologically defined muscle fibers within this spindle that we call nuclear bag fibers. And these fibers tend to have a more bulbous collection of nuclei in their central reach within that intrafusal muscle fiber. A muscle spindle might have a handful of these nuclear bag fibers and there may be equal number or more typically a smaller number of nuclear chain fibers. And these are a different type of intrafusal muscle fiber with respect to their morphology, but also their physiology. The morphological difference is that the nuclear chain fibers has their nuclei arranged typically in a single row along the central portion of that muscle fiber. So, rather there be than, so rather than there being more of a bulbous region that collects as a bag would a collection of nuclei. Rather, there's a chain a single row of nuclei that give this type of intrafusal fiber it's name. So, in addition to being morphologically distinct, there are differences between our nuclear bag fibers and our nuclear chain fibers with respect to their sensitivity to stretch. And how they contribute to our overall capacity of this spindle to monitor the length of the muscle. Imagine, for example, that we're applying a stretch to this muscle. So we're going from let's say length one to length two, and we do so over a relatively short period of time. Well, if we were to look at the nuclear bag fibers, what we would find is that the axons that supply those intrafusal muscle fibers will fire a bunch of action potentials especially during the change in length. And they won't be quite so modulated as we maintain a more stretched length. In contrast, the nuclear chain fibers, and more particularly, the group two axons that supply them they would be more concerned with the maintenance of the steady state that's then achieved, once that muscle is stretched to length number two. So, again, the nuclear bag fibers they're concerned with the dynamic aspects of movement. And the nuclear chain fibers are more concerned with reporting the steady state level that's achieved at the conclusion of the stretch. Now, as you've already seen, these muscle spindles are very important in giving rise to signals that we talk about in terms of proprioception. That is building up of an awareness of the movements of the body. And this awareness reaches consciousness via collaterals that enter the dorsal column medial lemniscal system, but there is also an important signal derived from these muscle spindles that supply to the cerebellum. So, recall that the cerebellum receives input via a spinal cerebellar pathway about the movements that the body is actually making. Well, this is one important source of information that is supplied to the cerebellum. Well, let's consider then how information derived from these group 1A and group 2A afferents is actually handled in the spinal cord. Well, the most common example that I trust you all have experienced at one time in your lives or another, is something called the myotactic reflex, or the stretch reflex. And one common way that this is elicited clinically is with the reflex hammer. So, what we see here is our typical knee-jerk reflex, where a force is applied to the patella tendon. And what's actually being done here with a tap of the tendon is a stretch is being applied to this quadricep muscle as that stretch is applied. It activates our group 1A axons that supplies the nuclear bag fibers in the muscle spindle. So, I say group 1A, because it's a very quick dynamic sort of stretch its supplied. And that's exactly the kind of stretch that the nuclear bag fiber in the group 1A afferent is going to signal. So, this sensory information runs back into the spinal cord? yes there are collaterals that enter the dorsal column region that allow us to make use of this information in central processing in higher levels above the spinal cord. But, for now, I want to focus in on what is going on in the spinal cord itself, that explains the knee-jerk reflex. Well, the output that produces the jerk involves a contraction of this quadricep muscle, right? So, in order to have contraction of this extensors of the leg we have to have a motor output from the relevant motor unit that supplies the very muscle that was stretched. And this happens because the afferent fiber makes a monosynaptic excitatory connection on this alpha motor unit. And so, let's just break down those terms. Monosynaptic means one synaptic connection, and it's excitatory. When the action potential arrives at that presynaptic terminal, there's the release of an excitatory neurotransmitter, probably glutamate or something like that, and a very strong synaptic connection exists here. Such that the activation of this sensory axon is very likely to lead to a super threshold depolarization of that motor unit and the firing of an action potential that leads then to the reflexive contraction of the muscle and the jerk of the leg. Well, in order to facilitate this behavior, things need to be just a bit more complicated. Now, there's also a flexor muscle, there in the hamstring region and in order to move this limb, ideally one would want to diminish the muscle tone that would be present in that hamstring muscle, such that the quadricep can actually extend the leg. Here's where an additional neuron is interposed between the sensory element and the relevant rotor element. And that additional neuron is an inhibitory interneuron. So this in inhibitory interneuron receives the excitatory input from this one a a afferent. And has the physiological action of inhibiting the motor output to the flexor muscle. So, this neuron right here then becomes diminished in its output to that flexor muscle. So, by decreasing the numbers of action potentials that is supplying that flexor muscle, the muscle tone of that flexor is now going to relax. And this removes the antagonism about this extensor movement of the leg. So, even one of our very most simple reflexes that we see in our central nervous system involves the coordination of excitation and inhibition to achieve functional synergy with the activation of one set of muscles, and the suppression of an antagonistic set. The result of this coordination is the smooth expression of movement. So, let's look at this from a more physiological perspective with micro electrode recordings. What we see is that, when there is a tap of the hammer on the patella tendon, we see in our sensory neuron an elicitation of a barrage of action potentials. So, that set of action potentials that leads to the activation of our motor neuron that is innervating our sensory muscles. So, this is monosynaptic exaltation of that motor unit. Now, there is also mono-synaptic exaltation of this Inhibitory interneuron. So, with the activation of that interneuron, then we see evidence of the suppression of the output to the antagonistic muscle, the flexor muscle. Notice, the suppression of activity that we see during the time that that sensory input is sending its signals into the circuitry of the spinal cord. So, we call this disynaptic inhibition of the motor neuron that supplies the flexor muscle. Sometimes, we call this pattern reciprocal inhibition because there is monosynaptic excitation to the synergist and disynaptic inhibition to the antagonist. So, we've been talking about the stretch reflex as we've commonly experienced it ourselves in a clinical examination with a hammer tap to the patella tendon, but I just want to make the point that this reflex is operating all the time. consider the challenge of holding steady a receptacle for some liquid that's being poured into it. So, what's going to happen now is as we want to maintain a steady angle here across our elbow joint we are going to be adding a load to the distal part of this biomechanical unit. So, that increase in load is going to stretch out this biceps muscle, and that stretch is going to be sensed by our 1a and group 2 afferents and its going to activate the very same kind of circuits that we just described in detail for the knee-jerk reflex. Only now, these circuits are in the cervical level of the spinal cord and they will provide output to the biceps muscle, which will cause a commensurate contraction across that elbow joint which will allow us to maintain this angle at a steady state position, even while the load is changing. And all of this is going to require the activation of synergistic muscles, and it's going to require the disynaptic inhibition of output to our antagonistic muscles, in this case our triceps. So let's see how this works. So, now we are adding a passive stretch which is due to the increased load that's being placed here on the distal part of the extremity. That's going to provide for a stretch signal in the muscle spindle and the communication back to this circuitry via the one a and group two a ferrets. And that leads to monosynaptic exotation, of the motor output to the synergistic muscles. And it's going to lead to disynaptic inhibition of the motor outflow, to the antagonistic muscles, and this allows for the increase in resistance. And the restoration of the joint angle that keeps us from spilling our our beverage. So this is an example in everyday life of how this circuitry works. So, in a more schematic form, we have some kind of goal that is set by our motor cortex. And that goal is communicated down through circuits that we'll described over the next several tutorials, and so this allows the output from the alpha motor neuron to scale the muscle to help achieve the goal of studying this receptacle against the changing load. So, as some disturbances now added, in the form of liquid coming into this receptacle, there is change in muscle length which is sensed by our muscle spindles and now afferent activity is fed back to the relevant alpha motor neurons, that then increase resistance against this changing load. Now, not depicted in this schematic is the disynaptic inhibition that allows for relaxation of the antagonistic muscles. But that two is part of the distribution of this incoming sensory information to the spinal cord circuitry.